Canine Pancreatitis: From Clinical Suspicion to Diagnosis and Treatment
World Small Animal Veterinary Association World Congress Proceedings, 2007
Thomas Spillmann, Dipl. vet. med., Dr. med. vet.
Professor of Small Animal Internal Medicine, Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, University of Helsinki

1. Introduction

Recent years have shown an increased research interest in diagnosis and treatment of canine pancreatitis which led to improvements in understanding the pathophysiology, efficient use of diagnostic procedures, and treatment success. However, the pancreas still remains the "hidden organ" and in individual cases right diagnosis and therapy is still challenging.

For canine acute pancreatitis, the etiology is varied and remains often unclear. Risk factors are obesity, fatty meals, hyperlipidemia (e.g., in miniature schnauzers), trauma, ischemia, severe intestinal diseases, systemic infections (e.g., babesiosis), endocrine disorders (e.g., hyperadrenocorticism, diabetes mellitus), certain toxins (e.g., scorpion venom, zinc), and drugs such as azathioprine, l-asparaginase, chlorpromazine, glucantime, tetracycline, and hydrochlorothiazide. The role of glucocorticoids as etiologic factor has been debated. It has been reported, that clinically suspected acute pancreatitis can be actually a sign of acute deterioration of chronic pancreatitis (1-4).

The etiology of chronic pancreatitis is less understood. Genetic predisposition, immune mediated processes or defect healing after an acute pancreatitis are seen as possible causes.

2. History and Clinical Signs Suggestive for Pancreatitis

There are no pathognomonic signs for acute or chronic pancreatitis. The severity of clinical signs and the clinical outcome depend on the severity and duration of pancreatic inflammation and its systemic consequences.

Gastrointestinal signs such as vomiting, diarrhea and cranial abdominal pain paired with apathy and anorexia can be caused by many underlying disorders. Of clinical importance is the fact, that the mild, edematous pancreatitis is often overlooked and treated successfully like a mild gastrointestinal disorder. Indication for more intensive diagnostic work up are signs of systemic involvement in the disease process such as weakness, dehydration, hypovolemia, fever, tachycardia, arrhythmia, jaundice, abnormal bleeding tendency, shock, or mixed dyspnea as a sign of respiratory distress. Very rarely, abdominal palpation can reveal a mass in the cranial abdomen.

Since necrotizing pancreatitis is commonly lethal without proper treatment it is advisable to suppose an acute pancreatitis when a patient with abdominal discomfort shows signs of systemic illness and to treat the case accordingly until otherwise proven by objective diagnostic procedures. In case of severe clinical signs blood pressure measurement is suggested to assess and control hypovolemic shock.

Chronic pancreatitis can be subclinical for whole life or eventually lead to endocrine or exocrine pancreatic insufficiency (EPI) as it is supposed to be the case with fibrous pancreatitis. With chronic recurrent pancreatitis, patients show episodes of abdominal discomfort and gastrointestinal signs of different severity. The latter is supposed to show also occasionally a more aggressive clinical picture resembling acute pancreatitis with sometimes lethal outcome. However, it is known from humans that "burned out pancreatitis" is associated with a decreased amount of pain episodes but diabetes mellitus and EPI.

3. Laboratory Tests

Since severe pancreatitis can lead to multi-organ disease/failure and finally death, hematology and clinical chemistry (liver, kidney, and metabolism profiles, electrolytes, blood gas analysis) are necessary to rule out other organ diseases than pancreatitis, and to assess severity of the disease process, extent of systemic complications, and prognosis. Possible systemic complications of acute pancreatitis that can be revealed by laboratory examinations are acute renal failure, acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). Hyperbilirubinemia can be a sign of extrahepatic biliary obstruction due to increased pancreatic size caused by inflammation, necrosis, pseudocysts or neoplasia.

Regular laboratory control examinations help to decide about treatment intensity and to check treatment success. Furthermore, assessment of diuresis and urinalysis belong to the clinical and laboratory profile in order to examine renal function and to reveal diabetes mellitus and diabetic ketoacidosis in association with pancreatitis.

Determination of canine C-reactive protein concentrations as a non-specific marker of inflammation seems to be of prognostic value since it is markedly increased in necrotizing pancreatitis (4).

Several laboratory tests have been used as "pancreas parameters" to find evidence for or against acute or acute-on-chronic pancreatitis in dogs. Serum parameters that were found to be of very low diagnostic value are canine trypsin-like immunoreactivity, canine α2-macroglobulin, canine α1-protease inhibitor-trypsin-complex and plasma or urine trypsinogen activation peptide (TAP). Other parameters currently used despite limitations in diagnostic value or accessibility are serum amylase and lipase activity and canine pancreatic lipase immunoreactivity (cPLI) (4).

Serum amylase and lipase activity originates mainly from the pancreas but also from other organs. Amylases are produced in intestine, liver, salivary glands and muscles. Lipases originate also from other sources e.g., gastric mucosa. Therefore, other diseases such as hepatopathies, diabetic ketoacidosis, and neoplasia or medications such as dexamethasone or glucantime, can lead to an increase in serum activity of both enzymes. Renal failure is also a cause of increased serum activities even without evidence of pancreatitis which makes differentiation difficult when diagnosing acute pancreatitis in uremic patients. It is also known that the values of both enzymes can be in the reference range although a patient suffers from acute pancreatitis. Studies revealed a sensitivity and specificity for amylase activity of 62.1% and 57.1%, respectively. They were for lipase activity 73.3% and 55.2%, respectively. The advantage of the parameters is their immediate availability using in-house tests. Their disadvantage is the high probability of false positive and false negative results with regard to an acute pancreatitis. There are no studies about their diagnostic value in chronic pancreatitis but it is supposed that there is even a higher amount of false negative results (4).

In recent years, a commercially available ELISA test for serum c PLI has been introduced and first publications and abstracts promise a better diagnostic value than for amylase or lipase activity. In contrast to serum lipase activity, canine pancreatic lipase seems to be of pancreatic origin only. Therefore increases in cPLI should reflect the release of the enzyme into the blood stream. The sensitivity for an acute pancreatitis was reported to be 81.8% but studies about specificity are still missing. It was reported, that serum cPLI is also elevated in patients with experimentally induced chronic renal failure. However, the values were still lower than an empirically chosen cut off value for pancreatitis of 250µg/l (2,5). Another abstract compared dogs with ultrasonographic changes of the pancreas with those that did have apparently normal pancreas. It was stated that cPLI had a sensitivity for pancreatitis of 49% in comparison to serum amylase activity with 71%, serum lipase activity with 50%, and cTLI with 9%. However, the study was biased by inclusion of dogs with acute and chronic pancreatitis (7).

A marker for the prognosis of acute pancreatitis could be the Urin-TAP-creatinine ratio in dogs. However, the TAP analysis is too laborious and expensive for regular diagnostic use (4).

Determination of lipase activity in abdominal fluid of patients with ascites seems to be a reliable marker for acute pancreatitis because it is significantly higher in dogs with ascites due to acute pancreatitis than in patients with ascites of other causes such as abdominal trauma, cardiac disease and intra abdominal neoplasia (7). However, only few patients with acute pancreatitis develop enough intraabdominal fluid for sampling and further analysis.

3. Imaging Techniques

Radiography is rarely diagnostic for pancreatic diseases. The imaging technique of choice is currently abdominal ultrasound due to its relatively high sensitivity and specificity. First sign of pancreatitis is an increased echogenicity of the pancreatic tissue. In cases of severe inflammation with pancreatic necrosis or abscess formation the pancreas shows a decreased echogenicity surrounded by an echodense margin of irregular shape. It can be difficult to differentiate pancreatic necrosis from pancreatic carcinoma with ultrasound only when the tumor has not metastasized into the liver yet. Pancreatic cysts or pseudocysts are echo free areas of different size within the pancreatic region. However, gas accumulation in the stomach and duodenum or severe abdominal pain can cause difficulties in assessing the pancreatic area with ultrasound. In case of easy accessibility of pancreatic changes by ultrasound fine needle aspiration for cytology and aspiration of fluid out of cysts or pseudocysts can be performed (9,10).

A more advance imaging technique with high diagnostic value for pancreatic diseases and their minimal invasive differentiation is contrast enhanced computed tomography. When available the technique is a big help to decide for and plan necessary surgical interventions (11).

4. Pancreatic Biopsy

Main indication for pancreatic biopsy is differentiation between necrosis and tumor and to diagnose chronic pancreatitis. Multiple biopsies should be taken via laparoscopy or laparotomy because of the patchy distribution of morphologic abnormalities in pancreatic diseases (12).

5. Treatment

The treatment can be divided into basic and problem oriented therapeutic measures. The aims are to reduce the secretion function of the pancreas, to minimize pain, and to avoid or control systemic complications. The basic treatment is according to the severity of the diseases process and contains following:

 No oral feeding for 3-5 days. However it was shown that postduodenal feeding via percutaneous gastrojejunal tube or nasojejunal tube improves the prognosis (13).

 Application of antiemetics (metoclopramide, ondansetron), H2-receptor blocker (e.g., ranitidine).

 Infusion therapy for rehydration and electrolyte substitution as needed (saline fluids), and for improvement of pancreatic microcirculation (dextrans).

 Analgetics (e.g., metamizole, dihydrocodeine, butorphanol, L-methadone, fentanyl-patch).

 Antibiotics (only with fever, signs of sepsis and pancreatic necrosis; possible combination for sepsis is metronidazole with enrofloxacin).

The intensity of additional, problem oriented therapy depends on the likelihood that the complication can be lethal. Complications that have to be addressed in an intensive care setting are treatment resistant pain, shock, acute renal failure, cardiac arrhythmia, DIC, ARDS, peritonitis, extrahepatic biliary obstruction and pancreatic abscess. Less dangerous complications are diabetes mellitus, pancreatic pseudocysts, and adhesions of the pancreas with adjacent organs (14).

Rarely found pancreatic pseudocysts can be emptied via ultrasound guided aspiration when they cause extrahepatic biliary obstruction or abdominal discomfort (15). In some cases they can resolve themselves. Pancreatic necrosis and abscesses should be controlled surgically when the lead to extrahepatic biliary obstruction or when the patient deteriorates despite intensive medical care. It is possible that even severe morphologic changes resolve spontaneously. However, there are no prognostic factors at time of diagnosis whether they will do or not. Repeated ultrasound examinations have to be performed to control treatment success and decide for or against a surgical approach. In case of surgical treatment, all necrosis should be removed and omentalization has seen to be of benefit (16). The patency of the common bile duct can be achieved by placing a rubber tube as a stent that is sutured with absorbable suture material to the duodenal wall (17). In case partial pancreatectomy has to be performed it is necessary that one third of the pancreas remains to maintain endocrine and exocrine function. Best results to maintain exocrine functions are achieved when performing an anastomosis of a pancreatic duct to the duodenum (18).

The treatment of chronic pancreatitis can only be symptomatic because its etiology is mostly unclear, the disease process is progressive and there are no curative therapies known. According to experiences from human medicine the aim of therapy should be relief of pancreatogenic pain and substitution of exocrine or endocrine insufficiency when it eventually occurs. In case of recurrent abdominal pain non-opioids (e.g., metamizole as suppository) can be given. When there is no response an opioid of low potency (e.g., dihydrocodeine) can be given orally. In rare cases combination of a non-opioid and an opioid of high potency (e.g., L-methadone) might be needed. The treatment should be given at the early beginning of a pain episode and accompanied by withdrawal of food for 1-2 days followed by gradual increased feeding of a low fat and highly digestible diet. It can be beneficial to maintain the diet for whole life. For people it is suggested to supplement pancreatic enzymes to extend the pain free intervals, but this approach is much under discussion. If the episode is very severe, hospitalization and treatment should be addressed as described for acute pancreatitis. It has to be stated, that these treatment recommendations are purely empiric and partly adopted from human medicine. There are no clinical studies in dogs that prove their efficacy (14).


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Speaker Information
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Thomas Spillmann, Dipl. vet. med., Dr. med. vet.
Department of Equine and Small Animal Medicine

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